ライフサイエンスコーパス: IgD

1 IgD and IgM are produced by alternative splicing of long

2 IgD CSR is a rare event, and its regulation is poorly un

3 IgD CSR occurred via both alternative nonhomologous end-

4 IgD deposition is difficult to diagnose, because routine

5 IgD has remained a mysterious Ig class and a bane to imm

6 IgD is also expressed at high levels on naive follicular

7 IgD monoclonal gammopathies are uncommon.

8 IgD overproduction was dependent on activation-induced c

9 IgD(-)CD27(-) double negative (DN) B cells with proinfla

10 IgD(hi) B cells induced IL-10 production by T cells and

11 IgD(hi) B cells may have a de novo versus induced regula

12 IgD(hi) regulatory B cells represent a novel regulatory

13 IgD/CD27 and CD24/CD38 core gating systems and an 11-col

14 IgD/CD27 and CD24/CD38 core gating systems were used to

15 PN significantly reduced lamina propria (1) IgD (naive), (2) IgDLPAM (antigen-activated homed to the

16 ternatively spliced Zfp318 exon 10 abolished IgD expression on marginal zone B cells, decreased IgD o

17 structural levels, much less is known about IgD.

18 similar recruitment of naive/early-activated IgD(+) IgM(+) B cells into both the brain and spinal cor

19 M-1) in naive B (IgD) and antigen-activated (IgD or IgM) B (CD45R/B220) cells.

20 4 and B cell-activating factor (BAFF), after IgD crosslinking.

21 In light-chain amyloidosis, IgD monoclonal proteins are found in ap-proximately 1% o

22 d Rac2, B cell development is arrested at an IgD- transitional B cell stage that we term transitional

23 odeling and PI3K/Akt and Erk signaling in an IgD-BCR-dependent manner.

24 When an IgD monoclonal protein is found, amyloidosis is often om

25 ated antibodies specific for CD43, CD11c and IgD (for GC enrichment) or GL7 (for non-GC enrichment);

26 from baseline in the frequency of CD20+ and IgD+/CD27- B cells, followed by reductions, although B c

27 nly cells and lacking expression of CD27 and IgD.

28 ervoirs within the germinal center cells and IgD(+)"naive" B cells in SAP-deficient mice, showing a p

29 ells induced IL-10 production by T cells and IgD(lo) B cells.

30 gD(-)CD27(+) class-switched memory (CSM) and IgD(+)CD27(-) naive B cells of HC (n = 48) and MS patien

31 including IgM ["IgM-only"], IgG and IgA) and IgD(-)CD27(-) cells ("double-negative," including IgM, I

32 ntibody isotypes (IgG(1) , IgG(4) , IgA, and IgD) may have a protective function; yet, their epitope-

33 e network that also encompasses IgM, IgG and IgD.

34 hed by low surface BAFF receptor and IgM and IgD B cell receptors.

35 Mature B cells coexpress both IgM and IgD B-cell antigen receptor (BCR) classes, which are org

36 rstanding how dual expression of the IgM and IgD BCR isotypes on mature naive follicular B cells tune

37 Intriguingly, the analysis of IgM and IgD expression by maturing and mature naive B cells demo

38 scripts, which would normally encode IgM and IgD from heterogeneous nuclear RNA transcripts via alter

39 emonstrate very distinct outcomes of IgM and IgD isotype activation in CLL cells, providing novel ins

40 ibrutinib effectively inhibited both IgM and IgD isotype signaling.

41 naive B cells expressing BCRs of the IgM and IgD isotypes respond to Ag in secondary lymphoid organs.

42 Most CLL cells express BCRs of IgM and IgD isotypes, but the contribution of these isotypes to

43 IgM and IgD receptor downmodulation, HS1 and ERK activation, che

44 ore investigated differences between IgM and IgD signaling in freshly isolated peripheral blood CLL c

45 lting in a switch from expression of IgM and IgD to expression of IgG, IgE, or IgA; this switch impro

46 s punctatus express two Ig isotypes: IgM and IgD.

47 dly, whereas swIg(+) and atypical IgM(+) and IgD(+) MBCs were stable over time.

48 lusters containing immunoglobulin (Ig) M and IgD that recruit the kinase Syk and transiently associat

49 Secretory delta mRNA and IgD(+) plasma cells were detected in all immune tissues

50 ferentiated B cells into CD138(+) plasma and IgD(-)CD27(+) memory cells and triggered immunoglobulin

51 egulation of IgD class-switched B cells and 'IgD-armed' basophils in autoinflammatory syndromes with

52 ic expansion of the transitional and anergic IgD(+)IgM(-)CD27(-) B cell subsets.

53 ntified through the use of anti-IgM and anti-IgD mAbs.

54 Moreover, anti-IgD-IC-loaded FDCs induced strong polyclonal IgM respons

55 lcium in response to either anti-IgM or anti-IgD cross-linking and contain a significantly increased

56 However, B cells were activated when anti-IgD-ICs, formed with Fc-specific rabbit anti-rat IgG, we

57 henotype (L-selectin and LPAM-1) in naive B (IgD) and antigen-activated (IgD or IgM) B (CD45R/B220) c

58 , increased populations of B-1 cells (B220(+)IgD(dim)IgM(+)CD43(+)CD24(+)CD5(+)), and higher numbers

59 CR (IgM-BCR) but not of the IgD-isotype BCR (IgD-BCR).

60 Human splenic and peripheral blood IgD(low/-) B cells also exhibit BD(L) regulatory activit

61 ted to ubiquitously express a membrane-bound IgD-superantigen.

62 equencing of human B cell subsets defined by IgD and CD27 expression: IgD(+)CD27(+) ("marginal zone [

63 ulation of mature B cells distinguishable by IgD(low/-) expression maintains tolerance by, at least i

64 se to certain pathogens and that the catfish IgD Fc-region, as has been suggested for human IgD, may

65 ation was progressively replaced by CD138(-) IgD(-) IgM(+) B cells, isotype-switched CD138(-) IgD(-)

66 -) IgM(+) B cells, isotype-switched CD138(-) IgD(-) IgM(-) memory B cells (B(mem)), and CD138(+) anti

67 127(-)FOXP3(+) regulatory T cells and CD19(+)IgD/M(+)CD27(-) B cells were increased through 5 years p

68 These modulations were mediated by CD19(+)IgD(low)CD38(+)CD24(low)CD27(-) B cells and needed direc

69 memory B cell subsets (CD19+IgD+CD27-, CD19+IgD+CD27+, or CD19+IgD-CD27+) at the single-cell level.

70 a low frequency of somatic mutations in CD19+IgD-CD27+ class-switched memory B cells in RV-specific m

71 We found an increased frequency of CD19+IgD+CD27+ unclass-switched memory B cells and a low freq

72 ets (CD19+IgD+CD27-, CD19+IgD+CD27+, or CD19+IgD-CD27+) at the single-cell level.

73 ulating naive or memory B cell subsets (CD19+IgD+CD27-, CD19+IgD+CD27+, or CD19+IgD-CD27+) at the sin

74 CD19(+), CD5(-), CD1d(-), IgD(hi) regulatory B cells from healthy controls produce

75 CD27(+)IgD(+)IgM(+) "natural effector" B cells showed reduced p

76 cells enriched in the CD24(int)CD38(+)CD27(+)IgD(-)IgM(+/low) subpopulation, which are able to transf

77 levels, whereas these were normal in CD27(+)IgD(-) memory B cells.

78 (-)IgD(+)CD38(+)), unswitched memory (CD27(+)IgD(+)CD38(-)), switched memory (CD27(+)IgD(-)CD38(-) or

79 27(+)IgD(+)CD38(-)), switched memory (CD27(+)IgD(-)CD38(-) or CD27(-)IgD(-)CD38(-)), and plasmablast

80 27(-)IgD(-)CD38(-)), and plasmablast (CD27(+)IgD(-)CD38(high)) subsets.

81 rtment, due to its exclusion from the CD27(+)IgD(+)IgM(+) subset, but this skewing does not affect th

82 equency of CD32B low/neg cells in the CD27(+)IgD(-) memory B cell subset and that these changes are a

83 equency of CD32B low/neg cells in the CD27(+)IgD(-) memory B subset in patients with RA.

84 n parallel to increased naive (CD19(+)CD27(-)IgD(+)) B-cell frequencies.

85 sing the proportion of naive B cells (CD27(-)IgD(+)CD38(-)) and concomitantly decreasing the immature

86 lating CD27(+) memory and memory-like CD27(-)IgD(-) double-negative (DN) B cells, but not CD27(-)IgD(

87 double-negative (DN) B cells, but not CD27(-)IgD(+) naive B cells.

88 tched memory (CD27(+)IgD(-)CD38(-) or CD27(-)IgD(-)CD38(-)), and plasmablast (CD27(+)IgD(-)CD38(high)

89 decreasing the immature transitional (CD27(-)IgD(+)CD38(+)), unswitched memory (CD27(+)IgD(+)CD38(-))

90 increased memory (P=0.02) and CD19+/CD27(-)/IgD(-) double negative (DN) B cells (P=0.02) and decreas

91 popolysaccharide (LPS) on apoptosis of CD27+ IgD- memory B (mB) cells from healthy controls.

92 CD27+IgD+ memory B cells and plasmablasts decreased only afte

93 decreased only after 532 days, whereas CD27+IgD- memory B cells were not affected, and there were no

94 B-cell immunophenotype (CD19/CD20/CD40(+)), IgD and/or IgM expression (67%), and lack of programmed

95 gs also reveal the existence of CD19(+)CD9(+)IgD(+) B-1 cells in the lungs of the muMT animals.

96 cell surface expression, it was named B-cell IgD low (BD(L)).

97 CD21(neg)) at the expense of mature B cells (IgD(+)IgM(+)CD21(+)).

98 xpansion of marginal zone (MZ)-like B cells (IgD(+)IgM(+)CD43(neg)CD21(+)CD24(+)), increased populati

99 of AF DENV(+) class-switched memory B cells (IgD(-)CD27(+) CD19(+) cells) reached up to 8% during acu

100 GC B cells (IgD(-)CD38(+)) were subdivided into 3 surface CD45RO fra

101 +)), and higher numbers of immature B cells (IgD(dim)IgM(dim)CD21(neg)) at the expense of mature B ce

102 sociated with a specific pattern of cellular IgD distribution resembling that observed in normal B ce

103 investigated interfaces from human IgA CH3, IgD CH3, IgG1 CH3, IgM CH4, T-cell receptor (TCR) alpha/

104 Circulating IgD bound to basophils through a calcium-mobilizing rece

105 se (AID) and generated local and circulating IgD-producing plasmablasts reactive to respiratory bacte

106 intact microbiome, against which circulating IgD, but not IgM, was reactive.

107 ss, CD19 deficiency did not affect early CNS IgD(+) B cell accumulation.

108 anscriptional repressor of CCL3 In contrast, IgD signaling induced activation of the cytoskeletal pro

109 Immunoglobulin D (IgD) is an enigmatic antibody isotype that mature B cell

110 pression on marginal zone B cells, decreased IgD on follicular B cells, and increased IgM, but only s

111 maturation was also affected, with decreased IgD(+)CD27(+) memory B cells while transitional B cells

112 Microbiota-dependent IgD CSR also was detected in nasal-associated lymphoid t

113 e routine immunofluorescence does not detect IgD.

114 , the activation (CD86) and differentiation (IgD, CD27, and CD38) profiles of B cells were measured l

115 evelopmental markers on peripheral blood DN, IgD(-)CD27(+) class-switched memory (CSM) and IgD(+)CD27

116 ota signal via Toll-like receptors to elicit IgD CSR.

117 early freezings of the WEHI-231 line express IgD but not CD93, which classifies the cells as more sim

118 ss membrane CD8, IgM, nor IgT, but expressed IgD on the cell surface.

119 elate with expansion of the T-bet expressing IgD(neg)CD27(neg)CD11c(+)CXCR5(neg) (DN2) pre-antibody s

120 ntal study data show that B cells expressing IgD at a low level (BD(L)) are a novel population of mat

121 subsets defined by IgD and CD27 expression: IgD(+)CD27(+) ("marginal zone [MZ]"), IgD(-)CD27(+) ("me

122 A targeted Zfp318 null allele extinguished IgD expression on mature B cells and increased IgM.

123 the immune system, as a critical factor for IgD expression.

124 d peptides showed a large spectra number for IgD, and immunohistochemistry showed intense glomerular

125 is showed 5% plasma cells, which stained for IgD.

126 intense glomerular and tubular staining for IgD.

127 Furthermore, B cells from IgD-deficient mice show defects in CXCL12-mediated CXCR4

128 s Eu-PKCbetaIItg mice displayed a shift from IgD(+)IgM(dim) toward IgD(dim)IgM(+) B cell populations

129 Furthermore, IgD expressed by IgM(-)/IgD(+) B cells preferentially as

130 e human upper respiratory mucosa to generate IgD-secreting B cells that bind respiratory bacteria and

131 defect in proliferative expansion of GL7(+) IgD(-) PNA(+) B cells in Ccnd3(-/-) mice defines an unde

132 rom failed proliferative expansion of GL7(+) IgD(-) PNA(+) B cells.

133 rm twice as many GC progeny as naive IgM(hi) IgD+ counterparts.

134 the marginal zone phenotype (B220(hi)IgM(hi)IgD(lo)CD21(hi)) and to some (CD19(-)CD5(hi)) T cells.

135 oire displayed as low levels of IgM and high IgD on anergic B cells, masking a varying proportion of

136 on activity (CD19(+)CD5(+)Thy-1(int)IgM(high)IgD(high)) that we name "initiator B cells." Analysis of

137 d approximately 70% of total spleen IgM(high)IgD(low) cells during peak infection in both wild-type a

138 lls with its repertoire signature but higher IgD or lower CD27 expression levels) thus appear as the

139 D Fc-region, as has been suggested for human IgD, may function as a pattern recognition molecule.

140 in autoinflammatory disorders such as hyper-IgD syndrome, indicating that IgD orchestrates an ancest

141 vaccine response and contained hypermutated IgD(+) B cells.

142 R clones of any immunoglobulin isotype (IgA, IgD, IgM, and IgG) in blood.

143 Other broader classes of antibodies (IgA1, IgD, IgE and IgM), however, differed in these motif regi

144 ion predominantly composed of surface IgM(+) IgD(+) cells residing in villi of the small intestine an

145 lyses revealed a tendency of activated IgM(+)IgD(+)CD27(+) B cells to migrate to B-cell follicles and

146 i) B cells expressed and maintained an IgM(+)IgD(lo)CD27(+)CD80(+) phenotype following immunization.

147 Burkitt lymphoma-like lymphoma (CD19(+)IgM(+)IgD(+) cells) leads to the development of clonal blastoi

148 set of diagnostic genes discriminating IgM(+)IgD(+)CD27(+) blood and splenic MZB cells from switched

149 nectomized subjects, who also have few IgM(+)IgD(+)CD27(+) B cells, had reduced antibacterial IgM.

150 uction of mu-alpha switch circles from IgM(+)IgD(+) naive human B cells, indicating its role as an Ig

151 ion during the transition from pre-GC (IgM(+)IgD(+)CD38(+)CD27(-)) to GCB cells was followed by a dra

152 memory B-cell characteristics of human IgM(+)IgD(+)CD27(+) B cells in that they share typical memory

153 d to be expressed at greater levels in IgM(+)IgD(+)CD27(+) compared with switched B cells in healthy

154 ority of Ig mutated B cells--including IgM(+)IgD(+)CD27(+) B cells--are post-germinal center (GC) mem

155 Moreover, IgM(+)IgD(+)CD27(+) B lymphocytes preferentially responded to

156 n B cells is the origin of the mutated IgM(+)IgD(+)CD27(+) B cells present in HIGM1 patients, and we

157 within the numerically dominant naive (IgM(+)IgD(+)CD27(-)) or transitional (CD10(+)CD27(-)) subsets.

158 The origin of IgM(+)IgD(+)CD27(+) (IgM memory) cells is controversial.

159 centrated within a small population of IgM(+)IgD(+)CD27(+) (nonswitched) memory cells rather than wit

160 ficiency display a marked reduction of IgM(+)IgD(+)CD27(+) B cells in blood, whereas their switched m

161 the development and/or maintenance of IgM(+)IgD(+)CD27(+) B cells in humans.

162 nd IFN-gamma caused differentiation of IgM(+)IgD(+)CD27(+) B cells into PCs, induced class switching

163 yndrome (HIGM1) support populations of IgM(+)IgD(+)CD27(+) B cells that express mutated Ig genes.

164 In contrast, the numbers of IgM(+)IgD(+)CD27(+) B cells were normal in the absence of TLR3

165 heavy-chain CDR3 size distribution of IgM(+)IgD(+)CD27(+) B cells were not affected in these patient

166 lvap results in a dramatic decrease of IgM(+)IgD(lo) B cells in both the spleen and the peritoneal ca

167 oietic Plvap deletion has no effect on IgM(+)IgD(lo) B cell numbers.

168 nctions of human peripheral blood (PB) IgM(+)IgD(+)CD27(+) B lymphocytes with somatically mutated IgV

169 Resting IgM(+)IgD(+)CD27(-) B cells from human tonsils were labeled wi

170 them with sequences cloned from sorted IgM(+)IgD(+) B cells from neonatal liver and both wild-type an

171 Further linking splenic IgM(+)IgD(+)CD27(+) B cells with production of T-independent I

172 We found that IgM(+)IgD(+)CD27(+) but not switched B cells were strongly red

173 Thus, by bolstering the IgM(+)IgD(+)CD27(+) B-cell subset, IRAK-4 and MyD88 promote op

174 these mutated B cells is unknown; the IgM(+)IgD(+)CD27(+) cells do not express AID and appear to acq

175 ap under the Chd5 promoter rescues the IgM(+)IgD(lo) B cell phenotype.

176 -)CD45R(-)CD19(-), which gives rise to IgM(+)IgD(low)CD45R(low)CD5(+)Mac-1(+)CD19(high)CD43(+)CD23(lo

177 antity of specific IgM correlated with IgM(+)IgD(+)CD27(+) B-cell frequencies.

178 lones consisted of class switched and IgM(+)(IgD(+)) members, a feature that correlated significantly

179 ile and highly diverse compartment of IgM(+)(IgD(+)) and class-switched memory B cells.

180 nalysis revealed a high similarity of IgM(+)(IgD(+))CD27(+) and IgG(+) memory B cells but also pointe

181 Catfish IgM(+)/IgD(+) B cells are small and agranular.

182 Comparatively, IgM(+)/IgD(+) B cells can express any of the four catfish IgL i

183 ly, all secreted IgD transcripts from IgM(+)/IgD(+) and IgM(-)/IgD(+) B cells were V-less and began w

184 In this study, IgM(+)/IgD(+) and IgM(-)/IgD(+) catfish B cell populations were

185 resembled pro-B cells, and were CD19(+)IgM(-)IgD(-)CD93(+)CD43(+)CD21(-)CD23(-)VpreB(+)CXCR4(+) Consi

186 For example, some catfish have <5% IgM(-)/IgD(+) B cells in their PBLs, whereas in others the IgM(

187 gD transcripts from IgM(+)/IgD(+) and IgM(-)/IgD(+) B cells were V-less and began with a leader splic

188 In this study, IgM(+)/IgD(+) and IgM(-)/IgD(+) catfish B cell populations were identified throug

189 Furthermore, IgD expressed by IgM(-)/IgD(+) B cells preferentially associates with IgL sigma.

190 er, these findings imply that catfish IgM(-)/IgD(+) B cells likely expand in response to certain path

191 In contrast, IgM(-)/IgD(+) B cells are larger and exhibit a plasmablast morp

192 membrane IgD transcripts from sorted IgM(-)/IgD(+) B cells contain viable VDJ rearrangements, with n

193 in their PBLs, whereas in others the IgM(-)/IgD(+) B cell population can represent as much as 72%.

194 ciencies have fewer immunoglobulin M (IgM)(+)IgD(+)CD27(+) B cells, a population that resembles murin

195 tors (TLRs) in homeostasis of human CD27+IgM+IgD+B cells.

196 oscopy, we demonstrated that endogenous IgM, IgD, and CD19 exhibited distinct nanoscale organization

197 In addition to enhancing mucosal immunity, IgD class-switched B cells enter the circulation to 'arm

198 The defects in CXCR4 signaling in IgD-deficient B cells can be overcome by anti-CD19 antib

199 ubdivided human tonsillar B cells, including IgD(-)CD38(+) GC B cells, into different fractions based

200 ion of secreted IgD resulting from increased IgD CSR exclusively within B cells of mucosa-associated

201 ey marker used to distinguish these cells is IgD, which, through alternative RNA splicing of H chain

202 pansions of immunoglobulin M (IgM)(+)kappa(+)IgD(low/-)CD21(low)CD27(+) B cells.

203 opulations, and of B cells naturally lacking IgD.

204 increased plasma BAFF and IFN-gamma levels, IgD(-)CD38(low)CD21(-)CD27(-) atypical B cells showed th

205 l virus and HIV-1 also exhibited an IgM(LOW) IgD(+) phenotype, which is associated with self-antigen

206 ell transfers revealed that anergic IgM(low) IgD+ B cells form twice as many GC progeny as naive IgM(

207 vidence for reactivation of anergic IgM(low) IgD+ IGHV4-34+ B cells and removal of cold agglutinin se

208 , including a major reduction of bone marrow IgD(+) cells, splenomegaly with a loss of white pulp and

209 ofile of bone marrow populations, and mature IgD+ B cells were enriched in sialylated bone marrow nic

210 cells demonstrated that this leader mediated IgD secretion.

211 CD79a and CD79b molecules, and all membrane IgD transcripts from sorted IgM(-)/IgD(+) B cells contai

212 smablast (IgD(-)CD38(++)CD27(+)) and memory (IgD(-)CD38(-)CD27(+)) transition.

213 In fact, most IgD(+) cells in the gills expressed CCR7.

214 Engagement of BCRs with rat-anti-mouse IgD (clone 11-26) does not activate B cells even when cr

215 ssion: IgD(+)CD27(+) ("marginal zone [MZ]"), IgD(-)CD27(+) ("memory," including IgM ["IgM-only"], IgG

216 cells occur exclusively in the anergic naive IgD(+), IgM(-) B-cell (BND) compartment.

217 unctionally attenuated (referred to as naive IgD(+)IgM(-) B cells [B(ND)]).

218 cGVHD patients was largely composed of naive IgD(+) B cells.

219 ty of CD23 molecules were expressed on naive IgD(+) B cells.

220 an tonsillar B cells demonstrated that naive IgD(+) and CD27(-) B cells are selectively induced to pr

221 s achieved through virus infection of naive (IgD(+)CD27(-)) B cells and their differentiation into me

222 lving CD27 to segregate naive B cells (NBC), IgD(+) unswitched (unsw)MBCs and IgG(+) or IgA(+) class-

223 ll subset is IgM(+), but due to low/negative IgD cell surface expression, it was named B-cell IgD low

224 ver, both IgA(+) and IgG(+) double negative (IgD(-) CD27(-)) CD11c(+) B cells were increased in ACPA(

225 modulating expression of surface IgM but not IgD BCRs, and by modifying basal calcium levels.

226 in infected cord blood cell cultures, and of IgD(-)CD27(+) cells (switched memory) in cell cultures f

227 Here, we describe a unique case of IgD deposition disease.

228 The diagnosis of IgD deposition disease underscores the value of laser mi

229 Recent discoveries of IgD in ancient vertebrates suggest that IgD has been pre

230 By showing dysregulation of IgD class-switched B cells and 'IgD-armed' basophils in

231 on between B cell subsets with enrichment of IgD(+)CD27(+) cells (commonly referred to as non-switche

232 V(-) children, the EBV-induced enrichment of IgD(-)CD27(+) B cells was significantly reduced in infec

233 rmore, we observed the specific expansion of IgD(+)CD27(+) B cells in response to gonococcal infectio

234 repressed the transcriptional expression of IgD and its regulator, Zfp318.

235 species of fish in which a secretory form of IgD has been characterized, and it occurs through the us

236 Also, the frequency of IgD-/CD27+ B cells increased in all tabalumab groups com

237 nt study, we reviewed the natural history of IgD-associated amyloidosis among 53 patients seen over 4

238 s upon Ag receptor cross-linking and lack of IgD expression, cells of the mouse cell line WEHI-231 ha

239 D receptor remains elusive, cross-linking of IgD on basophils stimulates release of immunoactivating,

240 l of IgM gene products and a virtual loss of IgD products.

241 The population of IgD(hi) B cells increased 3-fold as VL progressed.

242 specific role for Ampk in the regulation of IgD expression during B cell activation.

243 negative for surface IgM and retaining only IgD are autoreactive and functionally attenuated (referr

244 te from a unique population of IgM(+) and/or IgD(+) memory B cells that contain a high load of somati

245 ng other switched isotypes and rarely IgM or IgD, suggesting that IgE is derived from previously anti

246 matic increase during the GC-to-plasmablast (IgD(-)CD38(++)CD27(+)) and memory (IgD(-)CD38(-)CD27(+))

247 g increase in the number of genome-positive, IgD(-) B cells during chronic infection of both mouse st

248 In silico analysis of several published IgD genes suggested that this unique splicing mechanism

249 Regulation of rare IgD CSR events has been enigmatic.

250 Recently, IgD(-)CD27(-) (double negative, DN) and CD21(-)CD11c(+)

251 vy chain domain 1 as revealed by recombinant IgD/IgG chimeras.

252 ation, while accumulation of early-recruited IgD(+) B cells is CD19 independent.

253 Secreted IgD was found in two heavily glycosylated isoforms, whic

254 Interestingly, all secreted IgD transcripts from IgM(+)/IgD(+) and IgM(-)/IgD(+) B c

255 sed age-dependent overproduction of secreted IgD resulting from increased IgD CSR exclusively within

256 ovel strategy for the generation of secreted IgD.

257 and other innate immune cells with secreted IgD.

258 Our data demonstrate that secretory IgD is more prevalent and widespread across taxa than pr

259 ted in strong pCD79a and pPLCgamma2 signals, IgD stimulation only induced CD79a but not pPLCgamma2 ph

260 We show that TG2-specific IgD molecules are preferred in the reaction and that bin

261 Following anti-CD40 stimulation, IgD(-)IgM(+/low) B cells were blocked in their plasma ce

262 eded by accumulation of non-isotype-switched IgD(+) and IgM(+) B cells.

263 ith a significant expansion of all switched (IgD(-)) MBC and a decrease of naive B cells.

264 e examined circulating non-isotype-switched (IgD(+)CD27(+)) memory cells, a population that much evid

265 ferentially colonizing the isotype-switched (IgD(-)CD27(+)) memory B-cell pool.

266 flow cytometry, and RT-PCR demonstrated that IgD(+) B cell expression varies among individuals.

267 We have recently demonstrated that IgD(hi) B cells can occupy an extravascular perisinusoid

268 Based on these findings we hypothesize that IgD-expressing B cells using IGHV5-51 are preferentially

269 with periodic fever, our data indicate that IgD orchestrates an ancestral surveillance system at the

270 This indicates that IgD(+) B cells commonly found early in the CNS do not gi

271 such as hyper-IgD syndrome, indicating that IgD orchestrates an ancestral surveillance system at the

272 ught, and thus illustrate the potential that IgD may have a conserved role in immunity.

273 Also, transfection studies show that IgD functions as a typical BCR, because Igdelta-chains a

274 s of IgD in ancient vertebrates suggest that IgD has been preserved in evolution from fish to human f

275 ing, lack intron and exon sequences from the IgD (Ighd)-encoding region.

276 d intermediate isotypes or directly from the IgD(+) B cells.

277 ith healthy individuals, particularly in the IgD(-)CD27(-) memory B-cell population in ACPA(+) RA.

278 Intriguingly, the IgD(+)CCR7(+) population did not coexpress memIgM.

279 e insight into the enigmatic function of the IgD antibody.

280 ngated hinge found in immunoglobulins of the IgD isotype.

281 Although the nature of the IgD receptor remains elusive, cross-linking of IgD on ba

282 The specific role of the IgD-BCR is still enigmatic, but it is colocalized with s

283 the IgM-isotype BCR (IgM-BCR) but not of the IgD-isotype BCR (IgD-BCR).

284 These results show that the IgD-BCR, CD19, and CXCR4 are not only colocalized at nan

285 ptor CXCR4 is also found in proximity to the IgD-BCR.

286 i also interacted with B lymphocytes via the IgD B-cell receptor, resulting in internalization of bac

287 tivation after challenge with foreign Abs to IgD.

288 of infection or stimulation, in contrast to IgD(lo/neg) B cells.

289 anonical form of class switching from IgM to IgD occurs in the human upper respiratory mucosa to gene

290 ve B cells can be induced to class switch to IgD or that autoreactive B cells that use IgD as the B c

291 ies from B cells that have class switched to IgD via genetic recombination (and thus become class swi

292 cell-dependent and T cell-independent IgM-to-IgD class switching in B cells of the human upper respir

293 Taken together, IgD-binding NTHi leads to an unspecific immune response

294 displayed a shift from IgD(+)IgM(dim) toward IgD(dim)IgM(+) B cell populations in spleen, peritoneum

295 (+)) and IgG(+) MBC subsets and an unmutated IgD(+) MBC population.

296 to IgD or that autoreactive B cells that use IgD as the B cell receptor are not effectively deleted.

297 ade selectively in immature B cells, whereas IgD is coexpressed with IgM when the cells mature into f

298 Together, these findings are consistent with IgD deposition disease.

299 s developmentally regulated in parallel with IgD, with little in pro-B cells, moderate amounts in imm

300 Similarities with IgD(+)IgM(-) subsets in mammals are discussed.